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ascites/l tyrosine
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A tyrosine-specific protein kinase from Ehrlich ascites tumor cells.
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A protein tyrosine kinase that phosphorylates both alpha and beta subunits of inactivated (Na+,K+)-ATPase from dog kidney was purified about 500-fold from Ehrlich ascites tumor cell membranes. The enzyme required divalent cations Mn2+, Mg2+, or Fe2+ but was inhibited by Cu2+ or Zn2+. The purified
Comparison of tyrosine protein kinases in membrane fractions from mouse liver and Ehrlich ascites tumor.
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Tubulin was phosphorylated mainly at tyrosine residues by membranes from mouse liver and Ehrlich ascites tumor with ATP in the presence of MnCl2, ZnCl2, NaVO3, and Nonidet P-40 in an epidermal growth factor (EGF)- and insulin-independent manner. The tyrosine tubulin kinase activity in the tumor
Comparison of tyrosine phosphorylation of proteins by membrane fractions from mouse liver, Ehrlich ascites tumor and MH134 hepatoma.
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When membrane fractions from mouse liver, Ehrlich ascites tumor and MH134 hepatoma were incubated with [gamma-32P]ATP at 0 degree C in the presence of MnCl2, ZnCl2 and NaVO3, proteins were phosphorylated on tyrosines to a larger extent in liver membranes than in tumor membranes. Separation of
Amino acid supply and protein metabolism in Ehrlich ascites tumour cells. 2. Incorporation of 14C-tyrosine.
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The incorporation of 14C-tyrosine into protein of incubated Ehrlich ascites tumour cells was measured over a 10-fold range of external amino acid concentrations, the composition of which simulated that of mouse intraperitoneal fluid. Incorporation was linear with time and the rate of incorporation
Gene expressions of protein tyrosine phosphatases in regenerating rat liver and rat ascites hepatoma cells.
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mRNA levels for ten protein tyrosine phosphatases (PTPs), PTP-S, PTPH1, PTP-1, GLEPP1, LRP, PTP1D, PTPG1, PTP gamma, PTP delta, and LAR, were determined during regeneration of rat liver, and mRNA levels for 5 PTPs, PTP-S, PTP-1, PTP gamma, PTP delta, and LRP, were determined in three lines of rat
Stimulatory release of lipoprotein lipase activity with activation of protein tyrosine kinase produced by low molecular weight dextran sulfate in Ehrlich ascites tumor cells.
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Lipoprotein lipase (LPL), which is responsible for the hydrolysis of lipoprotein triacylglyceride, has been examined in Ehrlich ascites tumor cells. Low molecular weight dextran sulfate (DXS, M.W. 3.2 kDa) stimulates the release of the enzyme activity from the tumor cells into the incubation medium
The combination of the tyrosine kinase receptor inhibitor SU6668 with paclitaxel affects ascites formation and tumor spread in ovarian carcinoma xenografts growing orthotopically.
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OBJECTIVE
The purpose of this study was to investigate the antitumor activity of SU6668, tyrosine kinase inhibitor of vascular endothelial growth factor receptor 2 (VEGFR2), fibroblast growth factor receptor 1 (FGFR1), and platelet-derived growth factor receptor beta (PDGFRbeta), as single-agent
Involvement of protein tyrosine phosphorylation in the effect of green tea polyphenols on Ehrlich ascites tumor cells in vitro.
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Green tea extract and its polyphenolic components have been found to possess anticarcinogenic, antimutagenic, antihypertensive and antihepatotoxic effects, and several mechanisms have been proposed for these effects. In this study, the effects of five tea polyphenols, (-)-epigallocatechin-3-gallate
Involvement of protein tyrosine phosphorylation and reduction of cellular sulfhydryl groups in cell death induced by 1' -acetoxychavicol acetate in Ehrlich ascites tumor cells.
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Elucidation of the mechanisms underlying potential anticancer drugs continues and unraveling these mechanisms would not only provide a conceptual framework for drug design but also promote use of natural products for chemotherapy. To further evaluate the efficacy of the anticancer activity of
Inhibition of malignant ascites and growth of human ovarian carcinoma by oral administration of a potent inhibitor of the vascular endothelial growth factor receptor tyrosine kinases.
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We determined whether inhibition of the catalytic tyrosine kinase activity of the receptors for vascular endothelial growth factor/vascular permeability factor (VEGF/VPF) inhibits the formation of malignant ascites and the progressive growth of human ovarian carcinoma cells implanted into the
CCL18 from ascites promotes ovarian cancer cell migration through proline-rich tyrosine kinase 2 signaling.
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Ovarian cancer (OC) ascites consist in a proinflammatory tumor environment that is characterized by the presence of various cytokines, chemokines and growth factors. The presence of these inflammatory-related factors in ascites is associated with a more aggressive tumor phenotype. CCL18 is a member
Tyrosine kinase inhibition ameliorates the hyperdynamic state and decreases nitric oxide production in cirrhotic rats with portal hypertension and ascites.
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Tumor necrosis factor-alpha (TNF) causes vasodilatation and a hyperdynamic state by activating nitric oxide (NO) synthesis. Tyrphostins, specific inhibitors of protein tyrosine kinase (PTK), block the signaling events induced by TNF and NO production. A hyperdynamic circulatory syndrome (HCS) is
Effects of amino acids, analogs, and certain other agents in relation to tyrosine transport in sarcoma 37 ascites cells.
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COMPARISON OF THE INCORPORATION OF TYROSINE AND ITS IODINATED ANALOGS INTO THE PROTEINS OF EHRLICH ASCITES TUMOR CELLS AND RAT-LIVER SLICES.
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[Absorption of digitoxin by ascites (Ehrlich) tumor cells and effect on tyrosine-C14 protein incorporation].
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